1. Field of the Invention
The present invention is an implantable surgical device system and method for delivering therapeutic levels of energy to tissue in a living body. More specifically, it is a long-term implantable system and method for delivering therapeutic levels of ultrasound energy invasively within the body in order to treat chronic disorders associated with skeletal joints. Still more specifically, it is a long-term implant system and method for delivering therapeutic ultrasound energy to spinal joints, such as in particular intervertebral discs or associated bony vertebral structures.
2. Description of the Background Art
For many years, much research and commercial development has been directed toward delivering energy to tissue in order to achieve various desired therapeutic results. Examples of energy modalities previously described for tissue treatment include: electrical current (both DC and AC, e.g. radiofrequency or “RF” current), plasma ion energy, sonic energy (in particular ultrasound), light energy (e.g. laser, infrared or “IR”, or ultraviolet or “UV”), microwave induction, and thermal energy (e.g. convection or conduction). Other modalities for treating tissue include without limitation: cryotherapy (cooling tissue to desired levels to affect structure of function), and chemical therapy (delivering chemicals to the tissue to affect the tissue structure of function). Each of these energy delivery and other treatment modalities has been extensively studied and characterized as providing unique benefits, as well as unique issues and concerns, with respect to tissue therapy. Accordingly, many specific energy delivery methods and systems have been disclosed to provide unique benefits for particular intended therapeutic applications.
Various specific tissue responses to energy delivery have also been observed and reported during the course of significant study and characterization. In one regard, tissues or their function may be damaged by energy delivery such as thermal therapy. Examples of previously disclosed, differentiated effects of thermal tissue therapy generally characterized to damage tissue include, without limitation: ablation (which has been defined as either molecular dissociation or by achieving cellular necrosis), coagulation, degranulation, and desiccation. Alternatively, energy delivery in certain particular forms has also been characterized as promoting reproductive stimulation in certain tissues. Certain desired results have been disclosed with respect to intending controlled tissue damage with tissue thermal therapy; other desired results have been disclosed with respect to promoting tissue reproduction with tissue thermal therapy. In any event, because of the pronounced effects observed from tissue energy delivery, it is often desired to control and accurately select the localization of tissue/energy interaction in order to treat only the intended tissue, else normal surrounding tissue is effected with harmful results.
Accordingly, the different energy delivery modalities have been specifically characterized as providing particular benefits and problems versus other modalities with respect to various specific tissues and related medical conditions. Examples of specific medical conditions and related tissue that have been studied and characterized for tissue energy delivery include: tumors such as cancer (e.g. liver, prostate, etc.); vascular aneurysms, malformations, occlusions, and shunts; cardiac arrhythmias; eye disorders; epidermal scarring; wrinkling; and musculo-skeletal injury repair. The nature of the condition to be treated, as well as the anatomy of the area, can have significant impact on the desired result of energy delivery, which directly differentiates between the appropriateness or inappropriateness of each of the different energy delivery modalities for such application (as well as the corresponding particular operating parameters, systems, and methods for delivering such energy).
Depending upon the particular energy modality, various different parameters may be altered to affect the thermal effect in particular tissues, including which type of effect is achieved (e.g. ablation, coagulation, desiccation, etc.), as well as depth or degree of the effect in surrounding tissues. For the purpose of a general understanding, however, known tissue responses to thermal therapies, e.g. effect of changing temperatures to particular levels, have been previously characterized for certain tissues in prior disclosures which are summarized as follows.
As described above, temperature elevation of biological tissues is currently used for outright tissue destruction or to modify tissues to enhance other therapies. Low temperature elevations (41-45° C.) of relatively short duration (<30-60 min) have been disclosed as being associated with cell damage, but generally only to such extent to be repairable and considered non-lethal. In this range, it is believed that heat mediated physiological effects include heat induced acceleration of metabolism or cellular activity, thermal inactivation of enzymes, rupture of cell membranes, and delayed onset of increasing blood flow and vessel permeability. Prior disclosures addressing temperature exposures in excess of 45° C. and/or longer durations have stated that cellular repair mechanisms no longer function due to denaturation of key proteins or can't keep up with the accumulating damage. According to thermal therapy at such temperatures, complete cell death and necrosis have been observed in certain particular tissues to be fully expressed in approximately 3-5 days. Temperature exposures in the 42-45° C. regimen are commonly used for example as an adjuvant to radiation cancer therapy and chemotherapy, and have been considered for enhancing gene therapy and immunotherapy as well. Higher temperature elevations (50+° C.) have been investigated for inducing desirable physical changes in tissue, ranging from applications such as controlled thermal coagulation for “tightening” ligaments and joint capsules, tissue reshaping, and selective tissue thermal coagulation for destroying cancerous and benign tumors. High temperature exposures (50+° C.) are generally believed to produce rather lethal and immediate irreversible denaturation and conformational changes in cellular and structural proteins in various tissues, thereby thermally coagulating such tissues.
In general, heat-induced cell damage or tissue structural changes described above are believed to be attributed to thermal denaturation and aggregation of key protein structures. The accumulation of this thermal damage can be modeled using the Arrhenius rate process equation, which establishes a relationship between rate of thermal damage and the duration and temperature of exposure:
                                          1            τ                    =                      A            ·                          ⅇ                                                -                  Δ                                ⁢                                                                  ⁢                                  E                  /                  RT                                                                    ,                            (        1        )            where ΔE is activation energy (J mol−1), R is the universal gas constant (8.32 J mol−1 K−1), A is the rate constant (s−1), T is temperature in Kelvin, and 1/τ is rate of thermal damage (s−1). Using this expression (Eqn. 1), a relationship can be derived to determine an exposure time (τ2) and/or temperature elevation (T2) required to produce an equivalent observed biological effect associated with a specified temperature (T1) and time exposure (τ1). This is the basis of the thermal iso-effect equation as shown below, which is non-linear with respect to temperature exposure and linear with respect to exposure time:τ2=τ1e(ΔE/RT1T2)(T1−T2)=τ1K(T1−T2),  (2)where the parameter K is approximated as constant for typical therapeutic temperature elevations (10-30° C.). Furthermore, extensive in vitro and in vivo studies have demonstrated that ΔE for thermal damage is approximately constant at 140 J mol−1 for temperatures greater than 43° C. Thus, the relationship between time and temperature for a given biological effect depends upon activation energy only. Thus, as determined from the hyperthermia biology literature, K≅2 for T≧43° C. and K≅4-6 for T<43° C. The different values split at approximately 43° C. in order to model the biphasic behavior in the rate response, with faster damage accumulation after a break around 43° C. These values hold for lethal cellular damage, but not coagulation of structural proteins (collagen). Traditionally this iso-effect dose has been used to characterize hyperthermia cancer treatments with a target temperature elevation of 42.5-45° C., and has led to 43° C. becoming the historical reference dose temperature. This forms the basis of the thermal iso-effect dose (TID) equation, which as shown below can be used to calculate thermal dose of a varying temperature exposure over time as an equivalent exposure duration at 43° C. (or other reference temperature). Temperature time history is equated to a thermal dose at a known temperature reference.
                                          EM            43                    =                                                    ∫                0                                  t                  f                                            ⁢                                                K                                      (                                          T                      -                      43                                        )                                                  ⁢                                  ⅆ                  t                                                      =                                          ∑                                  t                  =                  0                                                  t                  final                                            ⁢                              Δ                ⁢                                                                  ⁢                                  tK                                      (                                          T                      -                      43                                        )                                                                                      ,                            (        3        )            where dt is a time step (min) and EM43 is thermal dose expressed in equivalent minutes at 43° C.
Various previously published disclosures have verified the Arrhenius model and the iso-effect relationship of different temperature-time exposures for generating trans-epidermal thermal necrosis in skin. Applying the TID analysis, a threshold of approximately 320 EM43 (wherein “EM” represents “equivalent minutes” at the given temperature shown in subscript) as found for temperatures between 44-60° C. Thermal dosages between 10-100 EM43 have been shown to correlate with improved response to hyperthermia and radiation therapy. For a conservative approach 250 EM43° C. is a threshold dose for complete thermal necrosis, where reported values range from 25-240 EM43° C. for brain and muscle tissue, respectively.
In addition, thermal coagulation or coagulation necrosis have been disclosed to occur in tissues exposed to temperatures greater than approximately 55° C. for a duration of minutes, in particular respect to collagen in certain structures studied. Thermal coagulation of soft tissues generally takes place only for temperatures in excess of 50° C. Numerous investigators have validated the “TID” (or “temperature iso-dose”) concept for predicting lesions using 240-340 EM 43° C. as a threshold dose and critical temperatures of 53-54° C. for coagulating muscle.